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International Immunology, Vol. 15, No. 9, pp. 1081-1087, September 2003
© 2003 Japanese Society for Immunology

TLR2 as an essential molecule for protective immunity against Toxoplasma gondii infection

Hye-Seong Mun1, Fumie Aosai1, Kazumi Norose1, Mei Chen1, Lian-Xun Piao1, Osamu Takeuchi3, Shizuo Akira3, Hiroshi Ishikura2 and Akihiko Yano1

1 Department of Infection and Host Defense, and 2 Department of Molecular Pathology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan 3 Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan

Correspondence to: A. Yano; E-mail: yano{at}faculty.chiba-u.jp
Transmitting editor: K. Sugamura

To investigate the role of the Toll-like receptor (TLR) family in host defense against Toxoplasma gondii, we infected TLR2-, TLR4- and MyD88-deficient mice with the avirulent cyst-forming Fukaya strain of T. gondii. All TLR2- and MyD88-deficient mice died within 8 days, whereas all TLR4-deficient and wild-type mice survived after i.p. infection with a high dose of T. gondii. Peritoneal macrophages from T. gondii-infected TLR2- and MyD88-deficient mice did not produce any detectable levels of NO. T. gondii loads in the brain tissues of TLR2- and MyD88-deficient mice were higher than in those of TLR4-deficient and wild-type mice. Furthermore, high levels of IFN-{gamma} and IL-12 were produced in peritoneal exudate cells (PEC) of TLR4-deficient and wild-type mice after infection, but low levels of cytokines were produced in PEC of TLR2- and MyD88-deficient mice. On the other hand, high levels of IL-4 and IL-10 were produced in PEC of TLR2- and MyD88-deficient mice after infection, but low levels of cytokines were produced in PEC of TLR4-deficient and wild-type mice. The most remarkable histological changes with infiltration of inflammatory cells were observed in lungs of TLR2-deficient mice infected with T. gondii, where severe interstitial pneumonia occurred and abundant T. gondii were found.

Keywords: MyD88, NO, TLR2, Toxoplasma gondii


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